Lecture 19 Using Exercise to Integrate Control of the Cardiovascular System PDF

Components of Vasculature: Review and Answer arteries → arteriole → capillaries → venule → vein Arteries • Deliver oxygenated blood to the tissues (aorta is largest) • Are thick-walled, with extensive elastic tissue and smooth muscle • Are under high pressure • The blood volume contained in arterie...

Components of Vasculature: Review and Answer arteries → arteriole → capillaries → venule → vein Arteries • Deliver oxygenated blood to the tissues (aorta is largest) • Are thick-walled, with extensive elastic tissue and smooth muscle • Are under high pressure • The blood volume contained in arteries is called the stressed volume Arterioles • Are the smallest branches of the arteries • Are the site of highest resistance to blood flow • Have smooth muscle wall that is extensively innervated by autonomic nerve fibers • Arteriolar resistance is regulated by the ANS • α-1 adrenergic receptors are found on the arterioles of the skin, splanchnic, and renal circulations • β-2 adrenergic receptors are found on arterioles of skeletal muscle 8 Components of vasculature: Review and Answer arteries → arteriole → capillaries → venule → vein Veins and Venules • Venules are formed from merged capillaries • Veins progressively merge to form larger veins. The largest vein, the vena cava, returns blood to the heart • Veins are thin-walled and are under low pressure • Veins contain the highest proportion of the blood in the cardiovascular system (large capacitance – 60-70%) • The blood volume contained in the veins is called the unstressed volume (meaning the blood volume under low pressure) • Veins have α-1 adrenergic receptors • Increased sympathetic nerve activity causes contraction of the veins which reduces their capacitance and therefore reduces the unstressed volume à increases venous return and gets more blood pumped into stressed volume. 9 Review: Neural Control of Cardiac Function • Gs-protein are coupled to β1/β2 adrenoceptors in the heart Heart β1=contraction M2 = relaxation • NE or Epi activation of β1/β2 leads to ↑ cAMP…activation of PKA… phosphorylation of L-type Ca2+ channels…↑intracellular Ca2+ • Net result: ↑inotropy ↑chronotropy ↑dromotropy ↑lusitropy • Gi-proteins are coupled to M2 muscarinic receptors in the SA and AV node of the heart • ACh activation of M2 leads to ↓ cAMP …inactivates PKA… ↓Ca2+ entry into cell…↑hyperpolarizing outward IK 10 Control of Vascular Tone by Catecholamines Vascular Smooth Muscle (arteries and veins) β2=relaxation α2 = contraction • Gs-protein are coupled to β2 adrenoceptors in vascular smooth muscle • NE or Epi activation of β2 leads to ↑ cAMP and relaxation • Ca2+-CaM activates myosin light chain kinase (MLCK) in vascular smooth muscle… phosphorylates myosin….. Contraction • However, MLCK is inhibited by cAMP • Gi-proteins are coupled to α2 adrenoceptors in vascular smooth muscle • NE activation of α2 leads to ↓ cAMP and contraction 11 Control of Vascular Tone by Catecholamines Vascular Smooth Muscle (arteries and veins) α1 = contraction • Gq-proteins are coupled to α1 adrenoceptors in vascular smooth muscle • IP3 pathway stimulates SR release of Ca2+ and activates protein kinase C (PK-C) via formation of diacylglycerol (DAG), which stimulates contraction 12 Epi and NE Affect Vascular Resistance a1 constriction Norepinephrine (≈ 20%) T1 T2 b1 T3 Sympathetic preganglionic neuron T4 T5 T6 T7 T8 Epinephrine (≈ 80%) T9 ­HR, contractility T10 T 11 a1 constriction T12 L1 L2 L3 Adrenal medulla a1, a2 NE ³ Epi b1, b2 Epi > NE b2 dilation (skeletal muscle) Epinephrine at low concentrations, Epi acts on β2 receptors and induces vasodilation in resistance vessels (β-adrenergic effect) at high concentrations, Epi acts on α1 receptors and induces vasoconstriction in resistance vessels (α-adrenergic effect) Norepinephrine Primary effect in all vascular beds is vasoconstriction Lungs!!!!!!!!!!!! 13 14 Overall cardiovascular response 15 Overall cardiovascular response to exercise 16 Answer 3 Parameter Control (pre exercise) Exercise Systolic BP 100 mm Hg 145 mm Hg Diastolic BP 70 mm Hg 60 mm Hg Heart rate 75 bpm 130 bpm Stroke volume (Est) 80 ml 110 ml Arterial Po2 100 mm Hg 100 mm Hg 40 mm Hg 25 mm Hg Venous Po • CO = SV X HR • COcontrol mL/min = 80 ml x 75 bpm = 6000 mL/min or 6 L/min • COexercise ml/min = 110 ml x 130 bpm = 14,300 mL/min or 14.3 L/min 2 • CO increased from 6 L/min à 14.3 L/min. • That is an 8.3 L/min increase (138% above control) • SV increased from 80 ml/beat to 110 ml/ beat • A 38% increase over control SV • HR increased from 75 à 130 bpm • A 73% increase over control HR • Thus, HR is more significant factor for increased CO. 20